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Bloody Diarrhea
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Blood
+ WBC
in stool
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· Salmonella: poultry
· Campylobacter: most common cause, associated with GBS
· E. coli 0157:H7—hemolytic uremic syndrome (HUS)
· Shigella: second most common association with HUS
· Vibrio parahaemolyticus: shellfish and cruise ships
· Vibrio vulnificus: shellfish, history of liver disease, skin lesions
· Yersinia: high affinity for iron, hemochromatosis, blood transfusions
· Clostridium difficile: white and red cells in stool
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Dx
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· best initial test is blood and/or fecal leukocytes
· Stool lactoferrin has greater sensitivity and specificity compared with stool leukocytes.
· The most accurate test is stool culture.
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Tx
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depends on 👾
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Giardiasis
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RF
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Exposure to contaminated food or water
Fecal incontinence & crowding (eg, daycare, nursing homes)
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Clx
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Acute
o Loose, foul-smelling, fatty stools
o Abdominal cramps
o Flatulence
o Weight loss
Chronic
o Malabsorption (eg, lactose intolerance)
o Profound weight loss
o Vitamin deficiencies
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Tx
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Metronidazole
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Vibrio vulnificus
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#
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· Gram-negative, free-living in marine environments
· Ingestion (oysters) or wound infection
· ↑ Risk in those with liver disease* (cirrhosis, hepatitis)
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S/s
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· Rapidly progressive (often <12 hours)
· Septicemia – septic shock, bullous lesions
· Cellulitis – hemorrhagic bullae, necrotizing fasciitis
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Dx
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Blood & wound cultures
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Tx
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IV ceftriaxone + doxycycline
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*Hereditary hemochromatosis is particularly high risk as iron acts as a growth catalyst.
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Typhoid fever
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Usually presents in a progressive manner
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S/S
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1st week: Fever.
2nd week: Abd pain + salmon-colored rash.
3rd week: HSM + Abd complications (bleeding – perforation).
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Clostridium difficile colitis
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RF
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Recent antibiotics / Hospitalization
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Path
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· Disruption of intestinal flora → C difficile overgrowth
· Exotoxins cause mucosal inflammation/injury
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Clx
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Watery diarrhea (most common)
Fulminant colitis/toxic megacolon (emergency 🚨)
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Dx
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Stool PCR
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Tx
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Oral metronidazole or vancomycin
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Viral Hepatitis
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👾
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· Hep A: Feco-oral
· Hep B + C: Blood / sex
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Path
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Viral infection of liver parynchma
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Clx
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· Jaundice + Fever
· Dark urine
· HSM
· weight loss, and fatigue
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Dx
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· LFT: ⤴️ direct bilirubin / ALP / AST&ALT
· Serology (for all except hep B):
· IgM antibody for the acute infection
· IgG antibody to detect resolution of infection.
· Disease activity of hepatitis C is assessed with PCR for RNA level
· Hep B: u know it
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Tx
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· Hepatitis A and E resolve spontaneously
· Tx only Hep C:
· Genotype 1: ledipasvir and sofosbuvir
· Other genotype: sofosbuvir and velpatasvir
· Tx of Chronic Hep B:
· positive for e-antigen with an elevated level of DNA polymerase, treatment is any one of the following: entecavir, adefovir, lamivudine, telbivudine, interferon, or tenofovir.
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Extra
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· If pt has fibrosis on Bx (Hep b / c): start tx
· In Hep C: If the PCR-RNA viral load is elevated, patients should be treated.
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Hepatitis C
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Dx
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· IgG + IgM
· PCR RNA
· Everyone born between 1945 and 1965 is tested for hepatitis C regardless of risk factors.
· Viral load testing has nearly eliminated the need for liver biopsy.
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Tx
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· If the PCR-RNA viral load is elevated, patients should be treated.
· If there is fibrosis on liver biopsy, initiating treatment becomes more urgent
· Genotype 1 is treated with sofosbuvir + ledipasvir orally for 12 weeks.
· The other genotypes are treated with sofosbuvir and velpatasvir orally.
· Interferon is only used in treatment failure.
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